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The 2016 National Task Force on Quality Nurse Practitioner Education described a preceptor as having the educational preparation or extensive clinical experience for clinical supervision. Preceptors are often unaware of teaching techniques, effective communication, and objective evaluation modes of student performance. Four 1-hour training modules for preceptors were developed to address these issues. Each illustrates communication and evaluation techniques to help nurse practitioner preceptors guide students as they learn to implement evidence-based practice. The online link to the continuing education training modules is provided for all interested schools of nursing, nurse practitioner preceptors, and other allied health professionals at no cost.

Successful daily self-management of diabetes is essential to the achievement of positive health outcomes. Basic to successful self-management of any disease is a sense of self-efficacy, or the feeling of confidence in one's self-management abilities. This study examined the association of these variables on the achievement of glycemic control, specifically A1C levels. This study used a retrospective cohort design to evaluate the predictive relationship of self-efficacy and self-care behaviors on A1C level. After Institutional Review Board approval was obtained, 60 medical records were accessed of people ≥ 18 years of age with type 1 or type 2 diabetes who were seen consecutively in a primary care practice located in an urban setting. Data analysis revealed no statistically significant relationships between global measures of self-efficacy and self-care and A1C levels. However, there were two questions from the Stanford Diabetes Self-Efficacy for Diabetes Scale found to be significantly related to A1C (P < 0.009). Those whose diabetes was well controlled were confident in selecting appropriate foods when hungry and in their ability to exercise for 15–30 minutes, four to five times per week. These findings, if replicated in future studies, may provide clinicians an opportunity to develop and test targeted self-management interventions yielding the highest probability of improved glycemic control.

Matrix metalloprotease (MMP)-9 is an elastolytic endopeptidase produced by activated macrophages that may be involved in the development of human pulmonary emphysema and could be inhibited with existing compounds. Mouse models have demonstrated that excess MMP-9 production can result in permanent alveolar destruction.To determine if MMP-9 causes cigarette smoke-induced emphysema using MMP-9 knockout mice and human samples.Mouse lungs were analyzed for inflammation and airspace enlargement using a mainstream smoke-exposure model. Human macrophage mRNA was isolated from subjects with emphysema by laser capture microdissection. Human blood monocyte mRNA was isolated from subjects with greater than 30 pack-year smoking history. Human gene expression was determined by quantitative polymerase chain reaction and compared with emphysema severity determined by automated computed tomography analysis. Plasma Clara cell secretory protein and surfactant protein-D were quantified to measure ongoing lung injury.Mice deficient in MMP-9 develop the same degree of cigarette smoke-induced inflammation and airspace enlargement as strain-matched controls. Macrophages are the predominant source of MMP-9 production in human emphysema specimens and similar quantities of macrophage MMP-9 mRNA is present in areas of lung with and without emphysema. Circulating monocytes produce more MMP-9 in individuals with advanced emphysema severity despite no correlation of MMP-9 with markers of ongoing lung damage.These results suggest that MMP-9 in humans who smoke is similar to smoke-exposed mice, where MMP-9 is present in emphysematous lung but not correlated with the emphysema. To the degree that the mechanisms of emphysema in humans who smoke resemble the mouse model, these data suggest specific inhibition of MMP-9 is unlikely to be an effective therapy for cigarette smoke-induced emphysema. Clinical trial registered with www.clinicaltrials.gov (NCT 00757120).

Cross-species analysis of microarray data has shown improved discriminating power between healthy and diseased states. Computational approaches have proven effective in deciphering the complexity of human disease by identifying upstream regulatory elements and the transcription factors that interact with them. Here we used both methods to identify highly conserved transcriptional responses during mechanical ventilation, an important therapeutic treatment that has injurious side effects. We generated control and ventilated whole lung samples from the premature baboon model of bronchopulmonary dysplasia (BPD), processed them for microarray, and combined them with existing whole lung oligonucleotide microarray data from 85 additional control samples from mouse, rat, and human and 19 additional ventilated samples from mouse and rat. Of the 2,531 orthologs shared by all 114 samples, 60 were modulated by mechanical ventilation [false discovery rate (FDR)-adjusted q value ( qFDR) = 0.005, ANOVA]. These included transcripts encoding the transcription factors ATF3 and FOS. Because of compelling known roles for these transcription factors, we used computational methods to predict their targets in the premature baboon model of BPD, which included elastin (ELN), gastrin-releasing polypeptide (GRP), and connective tissue growth factor (CTGF). This approach identified highly conserved transcriptional responses to mechanical ventilation and may facilitate identification of therapeutic targets to reduce the side effects of this valuable treatment.

Oxidative stress is a key element in the pathogenesis of emphysema, but oxidation of nucleic acids has been largely overlooked. The aim of this study was to investigate oxidative damage to nucleic acids in severe emphysematous lungs.Thirteen human severe emphysematous lungs, including five with alpha(1)-antitrypsin deficiency (AATD), were obtained from patients receiving lung transplantation. Control lung tissue was obtained from non-COPD lungs (n = 8) and donor lungs (n = 8). DNA and RNA oxidation were investigated by immunochemistry. Morphometry (mean linear intercept [Lm] and CT scan) and immunostaining for CD68 and neutrophil elastase also were performed.Nucleic acid oxidation was increased in alveolar wall cells in emphysematous lungs compared to non-COPD and donor lungs (p0.01). In emphysematous lungs, oxidative damage to nucleic acids in alveolar wall cells was increased in the more severe emphysematous areas assessed by histology (Lm,0.5 mm; p0.05) and CT scan (-950 Hounsfield units; p0.05). Compared to classic emphysema, AATD lungs exhibited higher levels of nucleic acid oxidation in macrophages (p0.05) and airway epithelial cells (p0.01). Pretreatments with DNase and RNase demonstrated that RNA oxidation was more prevalent than DNA oxidation in alveolar wall cells.We demonstrated for the first time that nucleic acids, especially RNA, are oxidized in human emphysematous lungs. The correlation between the levels of oxidative damage to nucleic acids in alveolar wall cells and the severity of emphysema suggest a potential role in the pathogenesis of emphysema.